Endocrine conditions Flashcards
Hypothyroidism: Presentation
Lethargy
Fatigue
Mood swings/low mood
Hair loss
High blood pressure
muscle stiffness and joint pain
cramping
painful menstruation
unexplained weight gain
paraesthesia
Hypothyroidism: pathophysiology
A thyroid hormone deficiency that causes metabolic processes to slow down. T3 and T4 are hormones which regulate the metabolism through affecting how the body uses energy and influencing heart rate, body temperature and mental activity as well as affecting he speed at which food moves though the digestive tract. Deficiency in these hormones means that metabolism slows down, heart rate decreases and pulse strength decreases in severe hypothyroidism.
Hypothyroidism: treatment and management
Medication for oedema if present.
Thyroid hormone replacement with levothyroxine. In extreme hypothyroidism - IV levothyroxine and hydrocortisone therapy.
Hyperthyroidism: Presentation
bulging eyes
weight loss
swelling of neck (goiter)
diaphoresis
heat intolerance
tremors
diarrhoea
anxiety
system specific presentations
Hyperthyroidism: Pathophysiology
overproduction of thyroid hormone produces a hormonal imbalance which can cause graves disease and various other types of hyperthyroidism. can be caused by excessive thyroid hormone ingestion (abusive or medical), benign nodules on glands, TSH tumours.
Thyrotoxic crisis/Thyroid storm
overproduction of thyroid hormones causes systematic adrenergic activity increase including epinephrine production and severe cardiac, respiratory and GI decompensation.
Hyperthyroidism: treatment and management
antithyroid drugs used when patients refuse other options. Radioactive iodine therapy aims to kill some thyroxine producing cells.
surgery in repeated cases to reduce size and thus activity of thyroid gland.
Types of diabetes
Type 1
Type 2
Gestational
secondary to disease/cause
Type 1 Diabetes: pathophysiology
Islets of Langerhans in the pancreas normally produce insulin (beta) and glucagon (alpha).
Endocrine area of pancreas is damaged or destroyed and thus alpha cells cannot produce sufficient insulin. This can occur due to genetic predisposition, auto-immune disease or environmental cause.
Lack of insulin means glucose is not removed from blood and taken up by cells, meaning the body functions as isn’t receiving enough glucose. This triggers the release of glucose from the liver into the blood stream.
Type 2 Diabetes: Pathophysiology
Insulin is produced by pancreas but cells become resistant to insulin as hormone cannot bind to binding sites on cells. Initially pancreas compensates by producing extra insulin but eventually demand is too high.
Type 2 diabetes: risk factors
Obesity
gestational diabetes
age
ethnicity
inactive lifestyle
family history
hypertension
Gestational diabetes
Development of diabetes in the 2nd or 3rd trimester of pregnancy. pregnancy hormones effect the body’s use of insulin and insulin resistance can develop. Normally resolves after delivery.
Diabetes: signs and symptoms
Polyuria
Polydipsia
weakness
fatigue
weight loss/gain without explanation
increased UTI
thrush
Hyperglycaemia: presentation
Increased HR
weak pulse volume
decreased temp
rapid and deep respiration
decreased blood pressure
dry skin
acetone in breath
diminished reflexes
Hyperglycaemia: treatment and management
Insulin for type 1 and 2 diabetes - used to decrease glucose metabolism and increase cellular metabolism
Hypoglycaemia: presentation
Increased HR
full pulse volume
shallow or normal respirations
clammy/sweating
moist skin
no acetone in breath
Hypoglycaemia: treatment and management
Glucose IV - directly into blood stream for rapid transport to cells for use
Glucagen - binds to glucagon receptors to trigger glucose molecule release into blood
Diabetic Neuropathy
Damage to nerves caused by hyperglycaemia, nerves become inflamed.
Commonly effecting the legs and feet a causes cramps, burning and numbness. This is initial peripheral neuropathy.
Can lead to nerve damage in the GI system, urinary tract and the heart.
DKA pathophysiology
Extreme hyperglycaemia crisis.
Insulin deficiency prevents glucose uptake by fat and muscle cells. Liver breaks down glycogen to meet demand. More glucose enters bloodstream. Excess glucose in bloodstream leads to glucose excretion in urine. Glucose starved cells break down protein and fat for energy. Fat breakdown produces fatty acids and glycerol which are broken down in the liver to produce ketones. Ketoacids cause acidosis. Proteins breakdown to produce amino acids which are broken down into urea and glucose. these processes cause hyper osmolarity and osmotic diuresis which causes severe dehydration, and acidosis causes tissue breakdown.
DKA: signs and symptoms
vomiting
fatigue
coma
shock
kussamals breathing
fruity smell on breath
polyuria
abdominal pain
DKA: treatment and management
IV fluids to correct dehydration and restore blood volume.
Insulin administered
electrolyte replacement
Urgent transfer to hospital
Osmotic diuresis
glucose concentration exceed maximum re-absorption capacity of kidney, glucose remains in filtrate and osmotic pressure increases. this pressure is an osmotic pull from cell to nephron lumen forces water and potassium to move out of cells and into urine.
Addisons disease: Early signs
polydypsia
polyuria
muscle weakness
craving salty foods
fatigue
weight loss
appetite loss
low mood
Addisons disease: late signs
Muscle cramps
Hypotension
Chronic exhaustion
irregular periods
nausea/vomiting
depression
